Acetylcholinesterase inhibitors and depressive symptoms in patients with mild to moderate Alzheimer’s Disease

Rozzini, Luca; Chilovi, Barbara Vicini; Bertoletti, Erik; Trabucchi, Marco; Padovani, Alessandro

doi:10.1007/bf03324693

Cited by 27 publications

(17 citation statements)

References 21 publications

(19 reference statements)

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“…These data corroborate other findings (Gauthier et al, 2002, Rozzini et al, 2006 showing a mildly positive effect on emotional symptoms in AD patients after treatment with ChEIs. This is the first study measuring in MCI patients the efficacy of cognitive rehabilitation therapy in association with ChEIs treatment.…”

Section: Discussionsupporting

confidence: 94%

Efficacy of cognitive rehabilitation in patients with mild cognitive impairment treated with cholinesterase inhibitors

Rozzini

Costardi

Chilovi

et al. 2006

Int J Geriat Psychiatry

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170

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Section: Discussionsupporting

confidence: 94%

Efficacy of cognitive rehabilitation in patients with mild cognitive impairment treated with cholinesterase inhibitors

Rozzini

Costardi

Chilovi

et al. 2006

Int J Geriat Psychiatry

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210

170

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“…Thus, depression should be carefully assessed and managed, particularly in those with more rapid decline who may have an increased risk of chronic or worsening depression. Since cognitive decline was associated with increased depression, it is possible that cognitive enhancers may improve or prevent depression secondary to the effect on cognition, as has been suggested in a preliminary study [39]. More research is needed to identify factors influencing the incidence and persistence of depression and its management in people with dementia.…”

Section: Discussionmentioning

confidence: 99%

Depressive Symptoms in Alzheimer’s Disease and Lewy Body Dementia: A One-Year Follow-Up Study

Fritze

Ehrt

Hortobágyi

et al. 2011

Dement Geriatr Cogn Disord

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Objective: To explore the course of depression in people with mild dementia and identify predictors for depression at 1-year follow-up. Methods: Patients with mild dementia (n = 199) were assessed using Montgomery and Åsberg Depression Rating Scale (MADRS) and the depression item from Neuropsychiatric Inventory (NPI) at baseline and after 1 year. A score above 6 on MADRS indicates at least mild depression. Linear and logistic regression analyses were performed to identify predictors of change in depression scores. Results: Among subjects with depression at baseline, 68.1% remained depressed at follow-up, whereas 31.9% had remitted, based on MADRS. Among patients without depression at baseline, 77.1% remained non-depressed at follow-up, whereas 22.9% had incident depression. The proportion with persistent depression was higher in the combined dementia with Lewy bodies (DLB)/Parkinson’s disease with dementia (PDD) group (45.5%) compared to AD (28%) (p < 0.05). Greater decline on the Mini Mental State Examination (p < 0.001) and higher baseline MADRS score (p < 0.001) were significant predictors of increased MADRS score. Conclusion: Two thirds of patients with depression at baseline were still depressed at follow-up, more so in DLB with PDD compared to AD. Cognitive decline was associated with worsening of depressive symptoms.

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“…Nicotine (Shearman et al, 2005; Tsukada et al, 2005) and anticholinesterase drugs such as galantamine (Noda et al, 2010; Schilstrom et al, 2007) and donepezil (Shearman et al, 2006), enhance extracellular levels of DA in the medial prefrontal cortex. In addition, anticholinesterase treatment presents AD properties (Tanaka et al, 2004; Rozzini et al, 2007; Cummings et al, 2008) and anticholinesterase augmentation of AD treatment improves the response in depressed patients (Pelton et al, 2008) and the release of DA in the prefrontal cortex (Wang et al, 2007a). The pro-cognitive effect of anticholinesterase drugs could rely on the synaptic potentiation of the D1/NMDA activation, since the D1 antagonist, SCH23390, and not the muscarinic acetylcholine receptor antagonist, scopolamine, reverses the cognitive improvement due to galantamine in an animal model of Alzheimer's disease (Wang et al, 2007b).…”

Section: All Antidepressants Increase Dopamine Levelsmentioning

confidence: 99%

A New Strategy for Antidepressant Prescription

Lavergne¹,

Jay²

2010

Front. Neurosci.

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From our research and literature search we propose an understanding of the mechanism of action of antidepressants treatments (ADTs) that should lead to increase efficacy and tolerance. We understand that ADTs promote synaptic plasticity and neurogenesis. This promotion is linked with stimulation of dopaminergic receptors. Previous evidence shows that all ADTs (chemical, electroconvulsive therapy, repetitive transcranial magnetic stimulation, sleep deprivation) increase at least one monoamine neurotransmitter serotonin (5-HT), noradrenaline (NA) or dopamine (DA); this article focuses on DA release or turn-over in the frontal cortex. DA increased dopaminergic activation promotes synaptic plasticity with an inverted U shape dose–response curve. Specific interaction between DA and glutamate is mediated by D1 receptor subtypes and Glutamate (NMDA) receptors with neurotrophic factors likely to play a modulatory role. With the understanding that all ADTs have a common, final, DA-ergic stimulation that promotes synaptic plasticity we can predict that (1) AD efficiency is related to the compound strength for inducing DA-ergic stimulation. (2) ADT efficiency presents a therapeutic window that coincides with the inverted U shape DA response curve. (3) ADT delay of action is related to a “synaptogenesis and neurogenesis delay of action.” (4) The minimum efficient dose can be found by starting at a low dosage and increasing up to the patient response. (5) An increased tolerance requires a concomitant prescription of a few ADTs, with different or opposite adverse effects, at a very low dose. (6) ADTs could improve all diseases with cognitive impairments and synaptic depression by increasing synaptic plasticity and neurogenesis.

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Acetylcholinesterase inhibitors and depressive symptoms in patients with mild to moderate Alzheimer’s Disease

Abstract: In depressed AD subjects, AChEis treatment improves depressive symptoms evaluated by GDS. This improvement is independent of cognition enhancement.

Cited by 27 publications

References 21 publications

Efficacy of cognitive rehabilitation in patients with mild cognitive impairment treated with cholinesterase inhibitors

Efficacy of cognitive rehabilitation in patients with mild cognitive impairment treated with cholinesterase inhibitors

Depressive Symptoms in Alzheimer’s Disease and Lewy Body Dementia: A One-Year Follow-Up Study

A New Strategy for Antidepressant Prescription

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